Premature birth represents about 13% of live births each year. Since lungs of these infants are underdeveloped, they receive supplemental oxygen right after birth, but little is known about its effects on the development of normal physiological responses and whether it impacts long-term cardio-metabolic function. Based on previous studies from our lab that showed increased pulse wave velocity in 12 month old rats exposed to neonatal supplemental oxygen, we hypothesized that neonatal exposure to supplemental oxygen causes cardiac hypertrophy and decreased left ventricular contractility. We also hypothesized that these effects to supplemental oxygen would be enhanced by 10 weeks on a high fat diet. To test the hypothesis, we used our rat model of 80% and 21% O2 exposed rats to FlO2=0.80 and 0.21 respectively, for 8 days post-birth. Two months after birth, these 80% and 21% rats were randomly assigned to either a high fat diet (60% of calories from animal fat) or low fat diet (CON) for 10 weeks during which their weights and caloric consumption were monitored. After 10 weeks, a Miller conductance catheter was inserted into the left ventricle to obtain pressure-volume loops and end-systolic pressure volume relationship, which was used to evaluate contractility. 80% rats exposed to CON diet showed higher cumulative weight gain than 21% rats on the same diet. No significant difference was observed between the weights of the left ventricles due to exposure to supplemental oxygen or high fat diet. Neonatal supplemental oxygen exposure decreased contractility whereas the combination of high fat diet and supplemental oxygen exposure reversed this effect. These data suggest that neonatal exposure to supplemental oxygen promotes weight gain and decreased ventricular contractility
